Exam 2 pt 2 Flashcards
Deadliest of all head injuries
Epidural hematoma
Epidural hematoma
Arterial bleeding that fills cranial cavity very quickly, compressing brain tissue (High pressure bleed)
Epidural hematoma often results in
brain injury and may lead to death (medical emergency)
Subdural hematoma occurs
following rupture of vessel–usually vein–between brain and dura (low pressure bleed)
3 types of subdural hematoma
Acute, subacute, and chronic
Most dangerous type of subdural hematoma
Acute
Time it takes for S&S of acute subdural hematoma to occur
Usually immediately
Time it takes for S&S of subacute subdural hematoma to occur
Days to weeks
Time it takes for S&S of chronic subdural hematoma to occur
Can take weeks
Subarachnoid/intraparenchymal hemorrhage is a result of
blood pooling inside brain
If subarachnoid/intraparenchymal hemorrhage is caused by trauma, it is usually accompanied by
DAI
Nontraumatic causes of subarachnoid/intraparenchymal hemorrhage
AVM
Chronic HTN
Brain tumors
Blood thinners
Subfalcal herniation
Herniation of the cingulate gyrus under the falx cerebri toward the opposite hemisphere
Uncal herniation
Herniation of part of the medial temporal lobe through the tentorial notch and is pressing the midbrain against the tentorium
Herniation causing decorticate posturing
Uncal herniation
Herniation causing decerebrate posturing
Tonsilar herniation
Decorticate posturing is due to
a lesion at the level of the midbrain separating the forebrain from the brainstem
Tonsilar herniation
One tonsil of the cerebellum herniates through the foramen magnum, compressing the medulla against the margin of the foramen
Decerebrate posturing is due to
lesion at the level of the lower brain stem separating the brain from the spinal cord
Normal ICP
5-10 mmHg
Etiology of stroke
Ischemic 80%
Hemorrhage 20%
Etiology of TBI
MVA
Signs and symptoms of stroke
Hemiplegia, unilateral, focal, neurologic
Signs and symptoms of TBI
Bilateral, focal, diffuse
Age in those with stroke
Old
Age in those with TBI
Young
Cost of severe stroke
$250,000
Cost of severe TBI
$4 mil
Recovery period for stroke
3-6 months
Recovery period for TBI
Years
Recovery pattern for stroke
Hypo- to hypertonicity
Recovery pattern for TBI
Rancho LOCF
Risk factors for stroke
Medical
Risk factors for TBI
Personality/lifestyle
Long term impairments/disability for stroke
Sensorimotor, cognitive
Long term impairments/disability for TBI
Cognitive, behavioral
Functional limitations for stroke
B/I ADL
Functional limitations for TBI
IADL
Permanent disability for stroke
70%
Permanent disability for TBI
90%
Reoccurrence for stroke
Low/medium 10%
Reoccurrence for TBI
High
Ability to predict outcome for stroke
Fair/good
Ability to predict outcome for TBI
Poor
Cerebral perfusion pressure
MAP-ICP
Normal CPP
70-100 mmHg
Do not treat if ICP is
Greater than 20-25
Medications used for increased ICP
Edema control
Anticonvulsants: seizure prophylaxis
Neuromuscular blockade/sedation
Types of meds for edema control (Increased ICP)
Osmotic diuretics
Steroids
Barbiturates (CNS depressant)
Other meds used for BI
Meds for agitation, seizures, and spasticity
Early signs of increased ICP: Consciousness
Confusion
Lethargy
Weakness
Restlessness
Early sign of increased ICP: Pupil
Sluggish
Early signs of increased ICP:Vision
Blurred/diplopia/decreased acuity, papilledema
Early signs of increased ICP: Motor
Contralateral paresis
Early signs of increased ICP: Vital signs
Stable
Early signs of increased ICP: Additional findings
Headache, nausea, seizures, CN palsy
Late signs of increased ICP: Consciousness
Coma
Late signs of increased ICP: Pupil
Fixed/dilated
Late signs of increased ICP: Motor
Abnormal posturing
Flaccid if herniation
Late signs of increased ICP: Vital signs
Acute increase in ICP causes compression of the cerebral blood vessels
Leads to cerebral ischemia
Leads to increase systemic blood pressure over the vasomotor center with simultaneous decrease in HR/RR (Cushing’s response)
Late signs of increased ICP: Additional findings
Headache
Vomiting
Changes in brain stem reflexes
3 types of cerebral edema
Vasogenic
cytotoxic
interstitial
Clinically most important type of cerebral edema
Vasogenic
How does vasogenic edema happen
Damage to BBB
Leads to inflammation
Leads to increase in permeability
How does vasogenic edema spread
Starts in area of injury and spreads and damages ipsilateral white matter
Focal neurologic deficits of vasogenic edema
Decrease in consciousness
How does vasogenic edema resolve
By slow diffusion
How does cytotoxic edema happen
Disruption of cellular metabolism
BBB is intact
Leakage of proteins and fluid from damaged blood vessels (grey matter)
What is interstitial edema
Rare non-communicating hydrocephalus
Breathing types
Cheyne-Stokes
Kussmal
Apneustic
Cheyne-Stokes
Periods of apnea followed by periods of hyperpnea
Kussmaul
Rhythmic, gasping, deep respiration associated with severe acidosis or coma
Apneustic
Prolonged slow inspirations, short expiratory phase
Cause of respiratory changes
Damage to respiratory centers (pons or upper medulla)
Removal of input from vagus nerve and pneumotaxic center in pons
Ventilator modes from most severe to least severe
Assist control
Synchronized intermittent mandatory ventilation
Continuous positive airway pressure (CPAP)
Assist control mode
Breathes for patient (ventilator overrides pt effort)
Synchronized intermittent mandatory ventilation mode
Breathes with patient (patient overrides ventilator)
Continuous positive airway pressure (CPAP) mode
Maintains open airway (patient must breathe on own)
PT role in ICU
Perform PT initial eval
Gain and maintain a clear chest
Prevent skin breakdown
Prevent loss of ROM
Stimulate consciousness
Sits at bedside/co-treat, even if patient is comatose or in persistent vegetative state
Part of team involved in family education
Minimally conscious state characteristics
Following simple commands Gestural yes/no responses Intelligible verbalizations Purposeful, non reflexive behavior Imaging: activation of appropriate CNS centers
Brain dead characteristics
No brain stem reflexes No response to pain No spontaneous respiration Flat EEG (not required) Usually confirmed by 2 independent physicians Organ donation possible
Persistent vegetative state characteristics
"disorder of consciousness" After 4 weeks of vegetative stage Brain stem function relatively intact Usually no ventilation Some response to simulation